1. Field of the Invention
The present invention relates generally to a surgical retractor which incorporates therein a blood flow monitor, and more particularly pertains to a neurological surgical retractor which monitors for the pressure of cerebral blood flow in the tissue adjacent to the retractor to prevent and minimize ischemic damage therein.
2. Discussion of the Prior Art
A variety of debilitating cerebral pathologies can now be treated by surgical procedures. Intracranial aneurysms, angiomas and certain types of tumors are among the many conditions which are surgically correctable. Often, a surgical instrument known as a retractor is used to give additional exposure of tissue in the operating field. Microsurgical techniques, which require extensive use of the light microscope, often require a version of the retractor known as the "Yasargil" or "self-retaining" retractor, while in other situations, a "hand-held" retractor is employed.
While use of these retractors, often for several hours, is necessary to expose the surgical site, surgeons and particularly neurosurgeons have worried that the pressure exerted on the delicate neurologic tissues can cause damage thereto. The neurosurgeon has traditionally relied on his experience and "feel" in setting a safe level of retractor pressure. This may prevent physical crushing or mechanical damage of the tissues, but of greater concern is the possibility of severely compromised local blood flow under the retractor head. This reduced blood flow could lead to oxygen starvation of the tissue cells called cerebral ischemia. This type of damage cannot be visually detected by the surgeon, even with the use of a microscope.
Cerebral blood flow may already be reduced during these surgical procedures due to a loss of autoregulation of the brain, cerebral edema, a mass lesion, induced hypotension, or fluctuations in arterial pCO.sub.2. This necessitates even more restraint in the use of excessive retractor pressures.
While damage due to retractor pressure has been suspected for many years, controlled studies to isolate this effect have appeared only recently. Numoto and Donaghy (1970) investigated the correlation between local pressure and electroencephalogram (EEG) changes. They concluded that "cortical electrical activity is suppressed as a result of changes in local blood flow which are in turn a result of local compression and tissue distortion."
Other EEG parameters have been shown to correlate with cerebral ischemia and could prove useful in evaluating or predicting damage caused by retractor pressure. Tolonen and Sulg (1981) found that the power in the delta band (0.0 to 4.69 Hz) of the EEG power spectrum correlated inversely with regional cerebral blood flow, such that an increase of EEG power in this band could warn of impending ischemic damage. Pronk and Simons (1982) concluded that the Hjorth time domain parameter of "mobility" (Hjorth, 1970) was sensitive to cerebral ischemia. Mobility is defined as the square root of the ratio between the variances of the EEG signal first derivative and the EEG amplitude. The ratio indicates average slope of the signal, and its square root, which is the standard deviation of the power spectrum along the frequency axis, indicates mean EEG frequency.
Rosenorn and Diemer (1983) applied various lead weights to the cortical surfaces of rats for fifteen or thirty minutes. Regional cerebral blood flow was determined by means of autoradiography with carbon-14 iodoantipyrine. Radiographic densitometry was determined by computerized image analysis. Blood flow immediately beneath the retractor was found to be dramatically lower than in surrounding regions (Table I). Others (Astrup et. al., 1981) have found that flow rates below 10 to 13 ml/100 gm/min lead to cell damage. Here, pressures as low as 20 mmHg for thirty minutes caused reduction of blood flow to 10-75 ml/100 gm/min and, presumably, ischemic damage.
Albin and co-workers (1975) attached a microcircuit strain gage to a retractor blade to measure applied pressure. A self-retaining retractor was applied for one hour, then released, and Evan's Blue dye was injected intravenously. Lack of blood brain barrier integrity was evaluated the extent of staining in brain sections. This procedure was repeated at five different pressure levels. Severe blood barrier compromise was found at pressures above 20 mmHg.
In a subsequent study (1977), Albin and co-workers compared somatosensory evoked potential amplitude with the pressure gradient (cerebral perfusion pressure minus brain retractor pressure), and found a direct relationship between these two factors. Pressures above only 10 mmHg were found to cause somatosensory evoked potential changes during induced hypotension. Induced hypotension is often used in neurosurgery to minimize the risk of an aneurysm rupture. These results showed that the pressure gradient was an effective predictor of brain damage, since a certain minimum level of cerebral perfusion pressure gradient assured adequate local blood flow. This parameter effectively compensated for variations in perfusion pressure, since the retractor pressure was continually adjusted to yield a constant pressure gradient.
Yokoh and co-workers (1981) investigated cerebral tissue damage in dogs using continuous and intermittent retraction. Evans' Blue staining and electroencephalogram power spectral arrays were examined after one hour of retraction. Six different pressure levels were used, and at each level, two groups of experiments were performed. The first group underwent continuous retraction for one hour. The second group was administered six cycles of retraction, each cycle consisting of ten minutes of retraction at the same level as the first group and five minutes of total release from pressure between cycles of retraction. Applied pressure was monitored with a strain gage apparatus attached to the self-retaining retractor.
Both power spectral arrays and morphologic studies showed marked superiority of the intermittent procedure over the continuous technique at each pressure level. The electroencephalogram power spectral array showed distinct recovery during each release phase of the intermittent retraction. The authors assumed that this finding was due to blood flow recovery under the retractor during release. They found that "the brain tolerates on average about 70% more intermittent retraction than continuous retraction from a morphological standpoint while electrophysiologically the difference is about 40%."
The "pressure" values reported by Yokoh cannot be directly compared with other studies because of the unfortunate choice of units. The values reported are in grams, a unit of mass of force, not pressure. A weight of certain mass was hung from the retractor tip before each experiment, the observed deflection was noted. A subsequent pressure level which caused an identical deflection would be reported as being pressure "equal" to the mass of the calibration weight. From the physical description the retractor used, the actual surface ar contact with the brain was probably around 120 mm.sup.2. Using this to convert Yokoh's gram values to units of pressure, the upper limit to pressure without damage in the continuous case was found to be 19 mmHg. In the intermittent case, it was found to be 30 mmHg.
Donaghy et. al. (1972) took the idea of retractor pressure monitoring one step farther. They developed an inflatable bladder which could be slipped over the end of a normal brain retractor blade. A pressure switch inside the bladder monitored applied pressure and acted as the feedback loop for an infusion-withdrawal pump connected to the bladder. Thus, if retractor pressure was too high, the pressure switch would close, causing withdrawal of air from the bladder and decreasing the applied pressure. If the retractor pressure was below the setpoint, air would be infused and more tissue would be exposed. The pressure setpoint could be maintained within about 5 mm of water limits with the device. Donaghy found electroencephalogram changes with pressures exceeding 250 mm of water (18.4 mmHg).
Rather than monitor absolute applied pressure or pressure gradient, Carter and co-workers (1978 and 1982) used a Peltier stack thermal diffusion probe placed on the cortical surface to more directly measure local blood flow. This device was calibrated by comparison with Xenon washout curves, and gave a quantitative output in units of ml/100 gm/min. The probe immediately detected compromised local blood flow which resulted when excess retractor pressure was applied.
Rosenon and Diemer (1983) showed that blood flow in the deeper areas of the brain (basal ganglia) was unaffected by retractor pressure which caused flow cessation in the surface cortical tissue. In addition, cortical grey matter requires four times more blood flow than the deeper white matter (Dripps, et al, 1982).
An indirect indicator of blood flow in tissue is the presence or absence of arterial and capillary bed pulsations which occur with each heartbeat. One method commonly used for detecting these pulsations is infrared densitometry. The infrared region of the electromagnetic spectrum extends from 690 nanometers to 300 micrometers in wavelength. As an increased volume of blood is forced into the capillary bed with each pulse pressure wave, the transmission of infrared light through the tissue is altered. This technique does not measure the flow of blood in a readily quantifiable way, but instead merely detects the peaks of the signals to measure the pulse rate. It should be noted, however, that such a system is known to evaluate the absence of appreciable blood flow. "Pulse watches" based on this technical approach are ineffective when capillary bed perfusion is reduced, such as when jogging in cold weather with unprotected hands. In such commercial devices, the fingertip or ear lobe is inserted into a light-tight enclosure or clip containing an infrared source and detector. The detector continuosly measures the amount of reflected or transmitted infrared light. A level detector circuit counts the reflection peaks for a defined period of time (usually a few seconds), then converts this count to a pulse rate (beats/minute). Such circuits have been incorporated into "pulse watches" for athletes, aerobic training participants, and hypochondriacs. In some of these devices, a finger clip is wired to the watch, or the finger is placed over the infrared emitter/detector area on the watch face when a pulse rate is desired.
Another related area of the prior art concerns oximeters for measuring the saturation of hemoglobin with oxygen in the blood. In a typical oximeter, two different infrared wavelengths of radiation are monitored, a first reference wavelength which is substantially unaffected by the saturation of hemoglobin with oxygen, and a second measurement wavelength which is very sensitive to the saturation of hemoglobin with oxygen. The signals obtained at the two different wavelengths of infrared radiation are then compared to determine the saturation of hemoglobin with oxygen in the blood. These prior art oximeters, however are not designed to, and do not measure the quantitative flow of blood.
Moreover, some existing experimental retractor designs use strain gages mounted on the retractor to measure the applied retraction force. While this is a step in the right direction, the damage caused by excessive retractor pressure is mostly a result of tissue ischemia secondary to reduced or obliterated blood flow in the tissue, and is not mechanical damage caused by the physical crushing of the tissue. The amount of retractor pressure needed to obliterate blood flow is not constant, but varies widely depending on anesthetic depth, systemic blood pressure, brain pathology, location of retraction, etc.
In summary, none of the prior art discussed hereinabove provides a surgical instrument provided with an effective contruction designed specifically to monitor blood flow in the tissue adjacent to the retractor to minimize and prevent ischemic damage therein.